Alcohol-induced liver injury represents a significant etiology of end-stage liver disease characterized inflammation, fat accumulation, and fibrosis. Because traditional treatment options such as organ transplantation have not been very successful, non-traditional therapies including the use of hepatic progenitor cells (HPC) offer an intriguing alternative. HPC proliferation and differentiation seems to be induced by two critical factors, hepatic insufficiency and a decreased ability of mature hepatocytes to replicate. Here, using two models of HSC proliferation, one initiated by inflammation due to Concanavalin A (ConA) and a second by fibrosis due to carbon tetrachloride (CCI4), each followed by partial hepatectomy, we will first determine whether the type of injury affects the differentiation lineage of HPCs. Next, since alcoholic liver disease (ALD) is complicated by fatty liver, we will determine the effect that fat, due to its reduction in the ability of mature hepatocytes to proliferate in response to injury, has on HPC proliferation in these models. It is hypothesized that fat accumulation will promote endogenous HPC proliferation by inhibition of normal hepatocyte function and proliferation within the inflamed or fibrotic and regenerating liver.